Evidence map›Paper›PMID 31638931›Full record

ArticleBMC cancer2019

Ectopic expression of BIRC5-targeting miR-101-3p overcomes bone marrow stroma-mediated drug resistance in multiple myeloma cells.

Jahangir Abdi, Nasrin Rastgoo, Yan Chen, Guo An Chen, Hong Chang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 24 citations in OpenAlex.

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  10. Research progress in proteasome inhibitor resistance to multiple myeloma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Jahangir AbdiDept. of Laboratory Hematology, Laboratory Medicine Program, Toronto General Hospital, University Health Network, 200 Elizabeth Street, 11E-413, Toronto, Ontario, M5G 2C4, Canada.
Nasrin RastgooDept. of Laboratory Hematology, Laboratory Medicine Program, Toronto General Hospital, University Health Network, 200 Elizabeth Street, 11E-413, Toronto, Ontario, M5G 2C4, Canada.
Yan ChenDept. of Laboratory Hematology, Laboratory Medicine Program, Toronto General Hospital, University Health Network, 200 Elizabeth Street, 11E-413, Toronto, Ontario, M5G 2C4, Canada.
Guo An ChenDepartment of Hematology/Oncology, First Affiliated Hospital, Nanchang University, Nanchang, China.
Hong ChangDept. of Laboratory Hematology, Laboratory Medicine Program, Toronto General Hospital, University Health Network, 200 Elizabeth Street, 11E-413, Toronto, Ontario, M5G 2C4, Canada. Hong.Chang@uhn.ca.
Toronto General Hospital · CANanchang University · CNUniversity Health Network · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultiple myeloma (MM) cells gain protection against drugs through interaction with bone marrow stromal cells (BMSCs). This form of resistance largely accounts for resistance to therapy in MM patients which warrants further exploration to identify more potential therapeutic targets.

methodsWe performed miRNA/mRNA qPCR arrays and western blotting to analyze transcriptional and translational changes in MM cells co-cultured with BMSCs. Drug cytotoxicity and apoptosis in MM

resultsWe found that BMSCs downregulated miR-101-3p and upregulated survivin (BIRC5) in MM cells. Survivin was downregulated by miR-101-3p overexpression and found to be a direct target of miR-101-3p using 3'UTR luciferase assay. Overexpression of survivin increased viability of MM cells in the presence of anti-myeloma drugs, and miR-101-3p inhibition by anti-miR against miR-101-3p upregulated survivin. Furthermore, overexpression of miR-101-3p or silencing of survivin triggered apoptosis in MM cells and sensitized them to anti-myeloma drugs in the presence of BMSCs overcoming the stroma-induced drug resistance.

conclusionsOur study demonstrates that BMSC-induced resistance to drugs is associated with survivin upregulation which is a direct target of miR-101-3p. This study also identifies miR-101-3p-survivin interaction as a druggable target involved in stroma-mediated drug resistance in MM and suggests it for developing more efficient therapeutic strategies.

Indexed as

Drug Resistance, Neoplasm3' Untranslated RegionsAntineoplastic AgentsApoptosisBortezomibCell AdhesionCell Line, TumorCell SurvivalCoculture TechniquesEctopic Gene ExpressionGene Expression Regulation, NeoplasticGene Knockdown TechniquesHEK293 CellsHumansMesenchymal Stem CellsMicroRNAs3' Untranslated RegionsAntineoplastic AgentsBIRC5 protein, humanBortezomibMicroRNAsMIRN101 microRNA, humanSurvivinApoptosisBone marrow stromamiRNAMulti-drug resistanceMultiple myelomaSurvivin

Identifiers

PMID31638931
PMCPMC6805455
OpenAlexW2981699389

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.